USP18 negative regulation of TBK1-IRF3 signaling contributes to HCMV infected malignant glioma
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- 英文论文题名：USP18 negative regulation of TBK1-IRF3 signaling contributes to HCMV infected malignant glioma
- 论文作者：Zhang Li
- 英文论文作者：Zhang Li ; Qingdao University
- 年：2016
- 作者机构：Qingdao University;
- 英文论文关键词：human cytomegalovirus ; glioma ; ubiquitination ; type I interferon
- 会议召开时间：2016-11-04
- 会议录名称：第十一届全国免疫学学术大会摘要汇编
- 英文会议录名称：Abstracts of 2016 CSI Congress on Immunology
- 语种：英文
- 分类号：R739.41
- 学会代码：IGMD
- 会议名称：第十一届全国免疫学学术大会
- 会议地点：中国安徽合肥
- 主办单位：中国免疫学会
- 学会名称：中国免疫学会
- 页数：2
- 文件大小：1296k
- 原文格式：D
- 会议级别：全国
摘要
Objective: Malignant glioma is the most frequently occurring primary tumor of the central nervous system, and represents one of the most lethal malignancies. Glioma cells show a stubborn resistance to several treatments, the etiology of malignant glioma remains obscure. Yet there are currently many studies over the potential involvement of viruses in malignant gliomas. Many studies reported that HCMV products were detected in malignant glioma, and correlated to tumor grade. HCMV stimulation with pathogen-associated molecular patterns triggering activation of the transcription factors,including NF-КB, IFN regulatory factor 3(IRF3) leads to the production of proinflammatory cytokines, type I IFNs, and induction of subsequent adaptive immune responses to exert anti-virus and anti-tumor effects. In this study, USP18 regulation on TBK1-IRF3-IFNβ signaling and its effect on malignant glioma activities were investigated.Methods: HCMV AD169 was utilized to infect human astrocytes, and whole genome transcriptome profile was conducted. In clinical malignant glioma specimens, we detected the virus in frozen tumor specimens by indirect immunofluorescence or in paraffin embedded tumor tissue specimens using the high sensitive immunostaining protocols and the expression of USP18 was also detected compared to paired normal tissues. TBK1-IRF3-IFNβ signaling was detected in cultured glioma cells. Results: results showed that the virus was detected in frozen tumor specimens and we also detected high expression of USP18 compared to paired normal tissues. TBK1-IRF3-IFNβ signaling was regulated by USP18 in cultured glioma cells. Conclusion: USP18 regulated TBK1-IRF3-IFNβ signaling and had effects on malignant glioma activities, which would provide new targets on treatment of malignant glioma
Objective: Malignant glioma is the most frequently occurring primary tumor of the central nervous system, and represents one of the most lethal malignancies. Glioma cells show a stubborn resistance to several treatments, the etiology of malignant glioma remains obscure. Yet there are currently many studies over the potential involvement of viruses in malignant gliomas. Many studies reported that HCMV products were detected in malignant glioma, and correlated to tumor grade. HCMV stimulation with pathogen-associated molecular patterns triggering activation of the transcription factors,including NF-КB, IFN regulatory factor 3(IRF3) leads to the production of proinflammatory cytokines, type I IFNs, and induction of subsequent adaptive immune responses to exert anti-virus and anti-tumor effects. In this study, USP18 regulation on TBK1-IRF3-IFNβ signaling and its effect on malignant glioma activities were investigated.Methods: HCMV AD169 was utilized to infect human astrocytes, and whole genome transcriptome profile was conducted. In clinical malignant glioma specimens, we detected the virus in frozen tumor specimens by indirect immunofluorescence or in paraffin embedded tumor tissue specimens using the high sensitive immunostaining protocols and the expression of USP18 was also detected compared to paired normal tissues. TBK1-IRF3-IFNβ signaling was detected in cultured glioma cells. Results: results showed that the virus was detected in frozen tumor specimens and we also detected high expression of USP18 compared to paired normal tissues. TBK1-IRF3-IFNβ signaling was regulated by USP18 in cultured glioma cells. Conclusion: USP18 regulated TBK1-IRF3-IFNβ signaling and had effects on malignant glioma activities, which would provide new targets on treatment of malignant glioma
Objective: Malignant glioma is the most frequently occurring primary tumor of the central nervous system, and represents one of the most lethal malignancies. Glioma cells show a stubborn resistance to several treatments, the etiology of malignant glioma remains obscure. Yet there are currently many studies over the potential involvement of viruses in malignant gliomas. Many studies reported that HCMV products were detected in malignant glioma, and correlated to tumor grade. HCMV stimulation with pathogen-associated molecular patterns triggering activation of the transcription factors,including NF-КB, IFN regulatory factor 3(IRF3) leads to the production of proinflammatory cytokines, type I IFNs, and induction of subsequent adaptive immune responses to exert anti-virus and anti-tumor effects. In this study, USP18 regulation on TBK1-IRF3-IFNβ signaling and its effect on malignant glioma activities were investigated.Methods: HCMV AD169 was utilized to infect human astrocytes, and whole genome transcriptome profile was conducted. In clinical malignant glioma specimens, we detected the virus in frozen tumor specimens by indirect immunofluorescence or in paraffin embedded tumor tissue specimens using the high sensitive immunostaining protocols and the expression of USP18 was also detected compared to paired normal tissues. TBK1-IRF3-IFNβ signaling was detected in cultured glioma cells. Results: results showed that the virus was detected in frozen tumor specimens and we also detected high expression of USP18 compared to paired normal tissues. TBK1-IRF3-IFNβ signaling was regulated by USP18 in cultured glioma cells. Conclusion: USP18 regulated TBK1-IRF3-IFNβ signaling and had effects on malignant glioma activities, which would provide new targets on treatment of malignant glioma
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